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BDNF - a key transducer of antidepressant effects.

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TLDR
Current data suggests that conventional antidepressants and ketamine mediate their antidepressant-like effects by increasing BDNF in forebrain regions, in particular the hippocampus, making BDNF an essential determinant of antidepressant efficacy.
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This article is published in Neuropharmacology.The article was published on 2016-03-01 and is currently open access. It has received 630 citations till now. The article focuses on the topics: Tropomyosin receptor kinase B & Brain-derived neurotrophic factor.

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Mechanisms of ketamine action as an antidepressant.

TL;DR: In this article, the mechanism of action of ketamine as an antidepressant, including synaptic or GluN2B-selective extra-synaptic N-methyl-D-aspartate receptor (NMDAR) inhibition, localized on GABAergic interneurons, inhibition of NMDAR-dependent burst firing of lateral habenula neurons, and the role of α-amino-3-hydroxy-5methyl-4-isoxazole-propionic acid receptor activation.
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Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation

TL;DR: The effect of acute and chronic inflammation on BDNF levels in the most common psychiatric and neurodegenerative disorders is focused on and some light is shed on the possible biological mechanisms that may influence this effect.
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How do antidepressants work? New perspectives for refining future treatment approaches

TL;DR: The ways in which monoamine neurotransmitter-based and neural plasticity theories reflect different or complementary approaches to antidepressant drug action are discussed, and how they might be integrated to offer novel solutions for people with depression are discussed.
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Dendritic Structural Plasticity and Neuropsychiatric Disease

TL;DR: The importance of recent genetic findings on the different mechanisms of structural plasticity are discussed and it is proposed that these converge on shared pathways that can be targeted with novel therapeutics.
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Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer.

TL;DR: The role of BDNF is illustrated as a potent protective factor that is able to confer protection against neurodegeneration, in particular in Alzheimer’s disease and how the involvement ofBDNF in the pathogenesis of brain glioblastoma has emerged is given, thus opening new avenues for the treatment of this deadly cancer.
References
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Journal ArticleDOI

The BDNF val66met polymorphism affects activity-dependent secretion of BDNF and human memory and hippocampal function

TL;DR: A role is demonstrated for BDNF and its val/met polymorphism in human memory and hippocampal function and it is suggested val/ met exerts these effects by impacting intracellular trafficking and activity-dependent secretion of BDNF.
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Antidepressant effects of ketamine in depressed patients

TL;DR: A first placebo-controlled, double-blinded trial to assess the treatment effects of a single dose of an N-methyl-D-aspartate (NMDA) receptor antagonist in patients with depression suggests a potential role for NMDA receptor-modulating drugs in the treatment of depression.
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A neurotrophic model for stress-related mood disorders.

TL;DR: Analysis of preclinical cellular and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies, are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation ofBDNF plays a role in the actions of antidepressant treatment.
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A Randomized Trial of an N-methyl-D-aspartate Antagonist in Treatment-Resistant Major Depression

TL;DR: Robust and rapid antidepressant effects resulted from a single intravenous dose of an N-methyl-D-aspartate antagonist; onset occurred within 2 hours postinfusion and continued to remain significant for 1 week.
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